MRS 1845Potent SOC inhibitor; blocks capacitative Ca2+ entry CAS# 544478-19-5 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 544478-19-5 | SDF | Download SDF |
PubChem ID | 11538542 | Appearance | Powder |
Formula | C21H22N2O6 | M.Wt | 398.41 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | <em>N</em>-Propylargylnitrendipine | ||
Solubility | DMSO : ≥ 83.33 mg/mL (209.16 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | 5-O-ethyl 3-O-methyl 2,6-dimethyl-4-(3-nitrophenyl)-1-prop-2-ynyl-4H-pyridine-3,5-dicarboxylate | ||
SMILES | CCOC(=O)C1=C(N(C(=C(C1C2=CC(=CC=C2)[N+](=O)[O-])C(=O)OC)C)CC#C)C | ||
Standard InChIKey | BITHABUTZRAUGT-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C21H22N2O6/c1-6-11-22-13(3)17(20(24)28-5)19(18(14(22)4)21(25)29-7-2)15-9-8-10-16(12-15)23(26)27/h1,8-10,12,19H,7,11H2,2-5H3 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Potent blocker of store-operated Ca2+ channels; inhibits capacitative Ca2+ influx in HL-60 cells (IC50 = 1.7 mM). |
MRS 1845 Dilution Calculator
MRS 1845 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.51 mL | 12.5499 mL | 25.0998 mL | 50.1995 mL | 62.7494 mL |
5 mM | 0.502 mL | 2.51 mL | 5.02 mL | 10.0399 mL | 12.5499 mL |
10 mM | 0.251 mL | 1.255 mL | 2.51 mL | 5.02 mL | 6.2749 mL |
50 mM | 0.0502 mL | 0.251 mL | 0.502 mL | 1.004 mL | 1.255 mL |
100 mM | 0.0251 mL | 0.1255 mL | 0.251 mL | 0.502 mL | 0.6275 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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IP3 and calcium signaling involved in the reorganization of the actin cytoskeleton and cell rounding induced by cigarette smoke extract in human endothelial cells.[Pubmed:25758670]
Environ Toxicol. 2016 Nov;31(11):1293-1306.
Smoking increases the risk of cardiovascular disorders and leads to damage caused by inflammation and oxidative stress. The actin cytoskeleton is a key player in the response to inflammatory stimuli and is an early target of cellular oxidative stress. The purpose of this study was to investigate the changes in actin cytoskeleton dynamics in human endothelial EA.hy926 cells exposed to cigarette smoke extract (CSE). Immunostaining revealed that CSE exposure resulted in modification of the actin cytoskeleton and led to cell rounding in a dose- and time-dependent manner. In addition, the intracellular calcium concentration was increased by treatment with CSE. Pretreatment with antioxidants (lipoic acid, glutathione, N-acetyl cysteine, aminoguanidine, alpha-tocopherol, and vitamin C) significantly attenuated the CSE-induced actin cytoskeleton reorganization and cell rounding. Calcium ion chelators (EGTA, BAPTA-AM AM) and a potent store-operated calcium channel inhibitor (MRS 1845) also reduced CSE-induced intracellular calcium changes and attenuated actin cytoskeleton reorganization and cell morphology change. Moreover, the CSE-induced intracellular calcium increase was suppressed by pretreatment with the inositol trisphosphate receptor (IP3R) inhibitor xestospongin C, the phospholipase C (PLC) inhibitor U-73122, and the protein kinase C (PKC) inhibitor GF109203X. These results suggest that reactive oxygen species production and intracellular calcium increase play an essential role in CSE-induced actin disorganization and cell rounding through a PLC-IP3-PKC signaling pathway. (c) 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1293-1306, 2016.
Calcium homeostasis and cone signaling are regulated by interactions between calcium stores and plasma membrane ion channels.[Pubmed:19696927]
PLoS One. 2009 Aug 21;4(8):e6723.
Calcium is a messenger ion that controls all aspects of cone photoreceptor function, including synaptic release. The dynamic range of the cone output extends beyond the activation threshold for voltage-operated calcium entry, suggesting another calcium influx mechanism operates in cones hyperpolarized by light. We have used optical imaging and whole-cell voltage clamp to measure the contribution of store-operated Ca(2+) entry (SOCE) to Ca(2+) homeostasis and its role in regulation of neurotransmission at cone synapses. Mn(2+) quenching of Fura-2 revealed sustained divalent cation entry in hyperpolarized cones. Ca(2+) influx into cone inner segments was potentiated by hyperpolarization, facilitated by depletion of intracellular Ca(2+) stores, unaffected by pharmacological manipulation of voltage-operated or cyclic nucleotide-gated Ca(2+) channels and suppressed by lanthanides, 2-APB, MRS 1845 and SKF 96365. However, cation influx through store-operated channels crossed the threshold for activation of voltage-operated Ca(2+) entry in a subset of cones, indicating that the operating range of inner segment signals is set by interactions between store- and voltage-operated Ca(2+) channels. Exposure to MRS 1845 resulted in approximately 40% reduction of light-evoked postsynaptic currents in photopic horizontal cells without affecting the light responses or voltage-operated Ca(2+) currents in simultaneously recorded cones. The spatial pattern of store-operated calcium entry in cones matched immunolocalization of the store-operated sensor STIM1. These findings show that store-operated channels regulate spatial and temporal properties of Ca(2+) homeostasis in vertebrate cones and demonstrate their role in generation of sustained excitatory signals across the first retinal synapse.
Dihydropyridines as inhibitors of capacitative calcium entry in leukemic HL-60 cells.[Pubmed:12527326]
Biochem Pharmacol. 2003 Feb 1;65(3):329-38.
A series of 1,4-dihydropyridines (DHPs) were investigated as inhibitors of capacitative calcium influx through store-operated calcium (SOC) channels. Such channels activate after ATP-elicited release of inositol trisphosphate (IP(3))-sensitive calcium stores in leukemia HL-60 cells. The most potent DHPs were those containing a 4-phenyl group with an electron-withdrawing substituent, such as m- or p-nitro- or m-trifluoromethyl (IC(50) values: 3-6 microM). Benzyl esters, corresponding to the usual ethyl/methyl esters of the DHPs developed as L-type calcium channel blockers, retained potency at SOC channels, as did N-substituted DHPs. N-Methylation reduced by orders of magnitude the potency at L-type channels resulting in DHPs nearly equipotent at SOC and L-type channels. DHPs with N-ethyl, N-allyl, and N-propargyl groups also had similar potencies at SOC and L-type channels. Replacement of the usual 6-methyl group of DHPs with larger groups, such as cyclobutyl or phenyl, eliminated activity at the SOC channels; such DHPs instead elicited formation of inositol phosphates and release of IP(3)-sensitive calcium stores. Other DHPs also caused a release of calcium stores, but usually at significantly higher concentrations than those required for the inhibition of capacitative calcium influx. Certain DHPs appeared to cause an incomplete blockade of SOC channel-dependent elevations of calcium, suggesting the presence of more than one class of such channels in HL-60 cells. N-Methylnitrendipine (IC(50) 2.6 microM, MRS 1844) and N-propargylnifrendipine (IC(50) 1.7 microM, MRS 1845) represent possible lead compounds for the development of selective SOC channel inhibitors.
Depletion of calcium stores regulates calcium influx and signal transmission in rod photoreceptors.[Pubmed:18755743]
J Physiol. 2008 Oct 15;586(20):4859-75.
Tonic synapses are specialized for sustained calcium entry and transmitter release, allowing them to operate in a graded fashion over a wide dynamic range. We identified a novel plasma membrane calcium entry mechanism that extends the range of rod photoreceptor signalling into light-adapted conditions. The mechanism, which shares molecular and physiological characteristics with store-operated calcium entry (SOCE), is required to maintain baseline [Ca(2+)](i) in rod inner segments and synaptic terminals. Sustained Ca(2+) entry into rod cytosol is augmented by store depletion, blocked by La(3+) and Gd(3+) and suppressed by organic antagonists MRS-1845 and SKF-96365. Store depletion and the subsequent Ca(2+) influx directly stimulated exocytosis in terminals of light-adapted rods loaded with the activity-dependent dye FM1-43. Moreover, SOCE blockers suppressed rod-mediated synaptic inputs to horizontal cells without affecting presynaptic voltage-operated Ca(2+) entry. Silencing of TRPC1 expression with small interference RNA disrupted SOCE in rods, but had no effect on cone Ca(2+) signalling. Rods were immunopositive for TRPC1 whereas cone inner segments immunostained with TRPC6 channel antibodies. Thus, SOCE modulates Ca(2+) homeostasis and light-evoked neurotransmission at the rod photoreceptor synapse mediated by TRPC1.